As described in commonly assigned U.S. Pat. No. 5,320,643, incorporated herein by reference, a cardiac pacemaker is an electrical device implemented to rectify an abnormal heart's natural pacing function by delivering appropriately timed electrical stimulation signals designed to cause the myocardium of the heart to depolarize. Stimulation pulses provided by implanted pacemakers usually have well-defined amplitude and pulse width characteristics both of which can be adjusted by remote programming and telemetry equipment to meet physiologic and device power conservation needs of the particular therapy regimen of a patient.
The amplitude and pulse width of the pacing pulses must be of such a magnitude above the stimulation threshold to maintain capture so as to prevent serious complications. Yet, it is desirable that these pacing output parameters are no higher than a reasonable safety margin above the stimulation threshold in order to prolong battery life. The patient's stimulation thresholds in the atrium and ventricle often fluctuate in the short term, and gradually change over the long term. Clinical experience has shown that the lowest stimulation threshold is observed immediately after implantation of the pacemaker. Inflammation of the cardiac tissue around the tip of the pacing lead electrode can drive the stimulation threshold up sharply during the first two to six weeks after implant to its highest level, depending on the lead used. When the stimulation threshold rises, a greater pacing pulse magnitude is required to effect capture. Some of the inflammation reduces over the long-term, to lower the threshold below the peak level, to the chronic threshold level. However, the chronic threshold usually never is as low as the acute level, since some permanent fibrous tissue remains around the electrode tip. Thus, care must be taken to ensure output levels are programmed to magnitudes that maintain capture. On a daily basis, thresholds may decrease with exercise, for example, and may increase with various activities, including sleep. Consequently, the safety margin is typically set by the physician on implantation of the pacemaker to accommodate projected maximal stimulation thresholds and may be adjusted manually by the physician or automatically by the pacemaker to accommodate these changes during follow-up sessions.
As described in commonly assigned U.S. Pat. No. 5,324,310, incorporated herein by reference, the post-operative determination of the stimulation thresholds by the physician typically requires the patient to be connected to surface ECG equipment while a threshold routine is conducted using the pacemaker programmer. The pacemaker programmer successively reprograms the pulse width and/or amplitude on a temporary basis to ascertain the points at which capture is lost. The pacing pulses are observed on a display or paper tracing as spikes, and capture or loss of capture is observed by the presence or absence of the evoked cardiac response wave shape (a P-wave or an R-wave) that follows each spike. At loss of capture, the programmed pacing pulse may be immediately restored so that the patient does not experience syncope. A strength-duration curve may be plotted from the resulting threshold data. The resulting threshold data may then be used to permanently reprogram the pulse magnitude. Naturally, such periodic patient studies are time-consuming and expensive to conduct. Moreover, they do not provide an indication of stimulation threshold fluctuation over the course of a patient's day and levels of activity. If, however, the pacing pulse is of a greater magnitude than necessary to meet these changing levels of activity, the life of the implantable pulse generator (IPG) is shortened as the battery is depleted.
As a result of these considerations, a great deal of effort has been expended over many years to develop IPGs with the capability of automatically testing the stimulation threshold, i.e. providing an “auto-capture” detection function, and resetting the pacing pulse magnitude to exceed the threshold by a safety margin without the need for clinical or patient intervention. A wide variety of approaches have been taken, for example, in commonly assigned '310 and '643 patents and in U.S. Pat. Nos. 5,165,404, 5,165,405, 5,172,690, 5,222,493 and 5,285,780.
In such IPGs, the capture detection approaches have taken a variety of forms typically in an attempt to overcome the difficulty in detecting the evoked cardiac response waveform shape from the pacing electrodes employed to deliver the pacing pulse. A high energy pacing pulse and the ensuing after-potentials and electrode/tissue polarization artifacts may mask the evoked response, and may also saturate the sense amplifiers coupled to the electrodes, until they dissipate. By the time that the sense amplifier is no longer blinded, the evoked response, if any, has typically passed the electrodes. Many of these approaches include blanking intervals for the sense amplifiers. Such approaches are combined with other efforts to suppress, attenuate, or compensate electronically for the composite post-delivery signal levels at the sense amplifier to shorten the saturation period (and the blanking interval) as much as possible.
Alternatively, the use of separate “far-field” EGM amplifiers and electrode systems from those “near-field” electrode systems used in delivering the pacing pulse have been proposed in, for example, the above referenced '310 patent.
In a further approach, one or more physiologic sensors that show a response to the mechanical action of the heart, e.g. a piezoelectric or impedance sensor, or a response that shows changes in physical properties of the blood when the heart is captured, e.g. blood pH, temperature, impedance or blood pressure sensors on the pacing lead have also been suggested as disclosed by the above referenced '643 patent.
The function and accuracy of the these approaches are impacted by one or more of factors including, but not limited to: myopotentials (electrical signals which are the product of muscle movement) in the case of EGMs; stray electromagnetic interference (EMI); problems with the sensor sensitivity (either too sensitive or not sensitive enough); and, in the case of pressure sensors, variations of the sensed electrical signals as a result of changes in thoracic pressure (for example, due to respiration, coughing or sneezing).
Further, in U.S. Pat. No. 5,601,615 issued to Markowitz et al, which is incorporated herein in its entirety, another approach is disclosed. Atrial loss of capture (ALOC) in response to an A-pace test stimulus is determined by the absence of a detected ventricular depolarization (V-event) in the latter portion of the paced A-V delay interval following the delivery of the A-pace test stimulus. In another approach for use in the atrium in patients having regular measured sinus rhythm, premature A-pace test stimuli are delivered. The presence or absence of a sensed A-event at the end of the measured sinus escape interval determines whether capture or loss of capture at the test stimulus is present.
In regard to the prior art known to the inventors, with the exception of the '615 patent, it is necessary to rely on additional components and circuitry that consume more energy and add to the bulk and cost of the system in addition to reliability concerns. Further additional components and circuitry are increased in dual chamber pacemakers, for example, where the difficulty of detecting the evoked P-wave is further complicated by its relatively low amplitude. Hence, there is a need for an apparatus and method to distinguish between the presence or absence of sinus node disease (SND) and/or AV conduction block. There is a further need for yet another apparatus and method that would enable to indicate and evaluate the presence or absence of atrial capture.